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Back in January, we were joined by Dr. Aubrey de Grey, Dr. Amutha Boominathan, Dr. Matthew O’Conner, and Michael Rae from the SENS Research Foundation for a webinar discussion panel focused on MitoSENS, the mitochondrial repair program. During the webinar, a number of points were discussed, and the Lifespan Heroes in the audience got to ask the researchers questions about MitoSENS and about the work of the SENS Foundation in general.

In 2015, the MitoSENS team raised funding on Lifespan.io to launch a study testing if they could create mitochondrial DNA copies in the cell nucleus, and they were successful in doing so as a result of the funds they received. In October 2019, the MitoSENS team launched a new follow-up project called MitoMouse, which aims to bring its mitochondrial repair therapy to mammals as a proof of concept on the road to translation to human use.

Many of us are fascinated by our various computing devices — our smartphones, our smart watches, and an ever-growing array of smart devices. What we sometimes forget is that we are biological creatures (at least, until The Singularity), and that even though biology as a discipline has been around much longer than computing, biology may yet supersede it.

If the 20th century was the era of computers, the 21st century may be the era of biology. And the two may even merge. Hello, synthetic biology and biological computing!

Last week SynBioBeta hosted The Global Synthetic Biology Summit, “where tech meets bio and bio meets tech.” People were urged to attend “to see how synthetic biology is disrupting consumer products, food, agriculture, medicine, chemicals, materials, and more.”

I’m excited to share I did an interview on transhumanism with Skyy John of Tipsy Bartender. He’s an actor and one the most famous people in the alcohol business!


We are about to live FOREVER because of new advances in technology and artificial intelligence! I sat down with futurist and transhumanist Zoltan Istvan as he explains how all of this will happen.

FIND ZOLTAN

A collaborative study published today in the journal Cell Reports provides evidence for a new molecular cause for neurodegeneration in Alzheimer’s disease. The study, led by researchers at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children’s Hospital, integrates data from human brain autopsy samples and fruit flies to reveal a novel mechanistic link between alterations in RNA splicing and tau-mediated neurodegeneration in Alzheimer’s disease.

“Cells carry out their functions by producing specific proteins encoded in their genes. To produce proteins, genes encoded in the DNA are first transcribed into RNA molecules, which subsequently are translated into proteins,” said corresponding author Dr. Joshua Shulman, associate professor of neurology, neuroscience and molecular and human genetics at Baylor and investigator at the Jan and Dan Duncan Neurological Research Institute.

In this study, Shulman and his colleagues investigated a molecular mechanism called RNA splicing that is involved in the production of mature RNA molecules necessary to produce working proteins. They looked into the possibility that aggregates of within neurons, a key marker of Alzheimer’s disease, interfered with RNA splicing.

Salamanders are renowned for their regenerative capabilities, such as growing back entire limbs. We can’t pull off this biological trick, but new research highlights a previously unknown regenerative ability in humans—one held over from our evolutionary past.

Our bodies have retained the capacity to repair injured or overworked cartilage in our joints, says new research published today in Science Advances. Remarkably, the mechanics of this healing process are practically the same as what’s used by amphibians and other animals to regenerate lost limbs, according to the study.

GenSight Biologics has recently released data showing the effectiveness of GS010, the company’s gene therapy for Leber Hereditary Optic Neuropathy (LHON), a mitochondrial disease that can lead to blindness. Like in previous studies, this therapy had a bilateral effect.

Gene Therapy

In LHON, the mitochondrial protein ND4 is poorly expressed through mitochondrial DNA (mtDNA). GS010 is a gene therapy that causes this protein to be allotropically expressed in the nucleus, after which it is shuttled to the mitochondria through messenger RNA. This makes GS010 a partial treatment for mitochondrial dysfunction, which is one of the hallmarks of aging.

Scientists are exploring how to edit genomes and even create brand new ones that never existed before, but how close are we to harnessing synthetic life?
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Scientists have made major strides when it comes to understanding the base code that underlies all living things—but what if we could program living cells like software?

The principle behind synthetic biology, the emerging study of building living systems, lies in this ability to synthesize life. An ability to create animal products, individualized medical therapies, and even transplantable organs, all starting with synthetic DNA and cells in a lab.

There are two main schools of thought when it comes to synthesizing life: building artificial cells from the bottom-up or engineering microorganisms so significantly that it resynthesizes and redesigns the genome.